A vexing Commentary on the important issue of aluminium and Alzheimer' disease

Abstract

The Commentary by Zatta [9] on our recent publication [4] is error strewn and interwoven with unsubstantiated claims which can only serve to blur the edges not only of the research published in our paper but also the general question of the role of aluminium in Alzheimer’s disease [2]. It is perhaps surprising that someone who has built his scientific reputation on the investigation of the putative role of aluminium in AD should now present such a prejudiced view. The essence of Zatta’s piece is immediately clear from its title. The use of the term ‘Vexata Questio’ implies that putting aluminium and AD together is to act in a malicious, irritating and even trivial manner. He is imploring the reader as to why he/she should have to waste his/her time considering aluminium and AD and not least because of new data [4] which he believes leaves more to the imagination than to the scientific method. His major unsubstantiated criticism is ‘modestly’ reiterated at the end of the Commentary and concerns the scientific method and statistical analyses. The research in our paper has been peer-reviewed and it is unfortunate that Zatta’s Commentary includes unsubstantiated opinions on its validity, opinions which can only serve to seed doubt in the scientific rigour of our findings. Another criticism with which he sought to reject our research was that the mineral water in question would include other constituents which could be responsible for the observed reduction in the body burden of aluminium. When challenged to explain this allusion he now reports in his Commentary that the 8.0 mg/L magnesium in Volvic could be responsible for the observed changes in the excretion of aluminium through an unsupported mechanism which he calls ‘the domino effect’. We have trawled through the literature on both animal and human studies to try to find one example of how drinking water containing 8.0 mg/L magnesium influenced the urinary excretion of aluminium. There are no data to support any such effects and presumably Zatta’s lack of any reference to such shows that he is aware of this. This does not, of course, prevent him from making this statement and using it along with his unsubstantiated criticisms of our scientific method as basis to reject our research. Zatta now turns his attentions to the general subject areas of aluminium, silicon and AD. I found his manner to be condescending and his reference to JD Birchall FRS ill-informed and unnecessary. He also gives the impression that he is unaware that what he calls ‘the old story’ has moved on and, as exemplified by our JAD paper, continues to this day, relying only upon sound science for its substance (see, http:// www.keele.ac.uk/depts/ch/groups/aluminium/publications.htm). However, Zatta’s understanding of the bioinorganic chemistry of silicon is very much an ‘old story’. It has been acknowledged for at least the last twenty years that there are no Si-C, Si-N, Si-O-C . . . etc. bonds in any form of life on Earth [8], though we are still looking for these up to this day, and therefore Zatta’s allusion to silicon being ‘usually bonded to glycoproteins’ is to say the least, ill-informed. The reference to the silicon concentration of blood is similarly out-dated, the lowest